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A genomic atlas of mouse hypothalamic development

ABSTRACT: The hypothalamus is a central regulator of many behaviors essential for survival such as temperature regulation, food intake and circadian rhythms. However, the molecular pathways that mediate hypothalamic development are largely unknown. To identify genes expressed in developing mouse hypothalamus, microarray analysis at 12 different developmental time points was performed. Developmental in situ hybridization was conducted for 1,045 genes dynamically expressed by microarray analysis. In this way, we identified markers that stably labeled each major hypothalamic nucleus over the entire course of neurogenesis, and thus constructed a detailed molecular atlas of the developing hypothalamus. As proof of concept for the utility of this data, we used these markers to analyze the phenotype of mice where Sonic Hedgehog (Shh) was selectively deleted from hypothalamic neuroepithelium, demonstrating an essential role for Shh in anterior hypothalamic patterning. Our results serve as a resource for functional investigations of hypothalamic development, connectivity, physiology, and dysfunction.

ORGANISM(S): Mus musculus

PROVIDER: GSE21278 | GEO | 2010/05/04

SECONDARY ACCESSION(S): PRJNA126583

REPOSITORIES: GEO

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A genomic atlas of mouse hypothalamic development

Project description:The hypothalamus is a central regulator of many behaviors essential for survival such as temperature regulation, food intake and circadian rhythms. However, the molecular pathways that mediate hypothalamic development are largely unknown. To identify genes expressed in developing mouse hypothalamus, microarray analysis at 12 different developmental time points was performed. Developmental in situ hybridization was conducted for 1,045 genes dynamically expressed by microarray analysis. In this way, we identified markers that stably labeled each major hypothalamic nucleus over the entire course of neurogenesis, and thus constructed a detailed molecular atlas of the developing hypothalamus. As proof of concept for the utility of this data, we used these markers to analyze the phenotype of mice where Sonic Hedgehog (Shh) was selectively deleted from hypothalamic neuroepithelium, demonstrating an essential role for Shh in anterior hypothalamic patterning. Our results serve as a resource for functional investigations of hypothalamic development, connectivity, physiology, and dysfunction. Affymetrix MOE430 microarrays were used to analyze the expression patterns of mouse hypothalamic and preoptic area tissues. The results were compared across the variables of Strain, Sex and Age.

2010-05-27 | E-GEOD-21278 | biostudies-arrayexpress

Single cell RNA-Seq identifies mechanisms controlling hypothalamic patterning and differentiation

Project description:The hypothalamus is a central regulator of many innate behaviors that are essential for survival, but the molecular mechanisms controlling hypothalamic patterning and cell fate specification remain poorly understood. To identify genes that control hypothalamic development, we have used single-cell RNA sequencing (scRNA-Seq) to profile mouse hypothalamic gene expression across 11 developmental time points between embryonic day 10 and postnatal day 45. This identified genes that delineated clear developmental trajectories for all major hypothalamic cell types and readily distinguished major regional subdivisions of the developing hypothalamus. We show that this approach can rapidly and comprehensively characterize mutants that control hypothalamic patterning and, in doing so, identify multiple genes that simultaneously repress posterior hypothalamic identity while promoting prethalamic identity. This argues in favor of a modified columnar organization of hypothalamus and prethalamus. These data serve as a resource for further studies of hypothalamic development, physiology, and dysfunction.

2020-08-09 | GSE132355 | GEO

Decoding the origin of neuronal diversity in hypothalamus by single-cell RNA-seq

Project description:The hypothalamus is one of the most complex brain structures whose development involves a plastic process of neuronal fate specification. Progress has been made to decipher the gene regulatory programs that are responsible for hypothalamus development; however, the molecular developmetal trajectory of hyothalamus is largely unknown. To understand how pre- and postmitotic transcriptional programs interact and coordinate to endow neuronal cell subtypes with their characteristic properties during hypothalamic development, we performed single-cell RNA sequencing (scRNA-seq) on single cells derived from Rax+ hypothalamic neuroepithelium at four critical developmental points during hypothalamic development. Our single-cell analysis provides a developmental landscape of mouse hypothalamus. We show that while the fate of radial glial cells (RGCs) is predetermined before differentiation but lack spatial code to distinguish from each other, different clusters of intermediate progenitors (IPCs) emerge to display diversifying fates and subdivide hypothalamic primordium into distinct spatially-restricted progenitor domains. We further characterize the maturation dynamics of hypothalamic neurons and suggest that immature neurons could evolve into multiple peptidergic neuronal subtypes. Finally, we identify sets of transcription factors (TFs) serving as regulons to determine the fate of diverse GABAergic and Glutamatergic neurons in hypothalamus. Together, our study offers a single-cell transcriptional framework for the hypothalamus developmental trajectory and propose a cascade diversifying model to deconstruct the origin of neuronal diversity in hypothalamus.

2021-08-05 | GSE151060 | GEO

Foxd1 is required for terminal differentiation of anterior hypothalamic neuronal subtypes

Project description:Although the hypothalamus functions as a master homeostat for many behaviors, little is known about the transcriptional networks that control its development. To investigate this question, we analyzed mice deficient for the Forkhead domain transcription factor Foxd1. Foxd1 is selectively expressed in neuroepithelial cells of the prethalamus and hypothalamus prior to the onset of neurogenesis, and is later restricted to neural progenitors of the prethalamus and anterior hypothalamus. During early stages of neurogenesis, we observed that Foxd1-deficient mice showed reduced expression of Six3 and Vax1 in anterior hypothalamus, but overall patterning of the prethalamus and hypothalamus is unaffected. After neurogenesis is complete, however, a progressive reduction and eventual loss of expression of molecular markers of the suprachiasmatic, paraventricular and periventricular hypothalamic is observed. These findings demonstrate that Foxd1 acts in hypothalamic progenitors to allow sustained expression of a subset of genes selectively expressed in mature neurons of the anterior hypothalamus.

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A single-cell RNA-seq analysis of molecular characterization of hypothalamic progenitor cells

Project description:To define molecular and cellular heterogeneity of progenitor cells in the developing mammalian hypothalamus, single cell RNA-sequencing (10x Genomics Chromium) was performed in embryonic human hypothalamus (GW10). We identified four major cell populations, including hypothalamic progenitor cells (HPCs), Glutamatergic neuronal cells, GABAergic neuronal cells and neuropeptidergic neurons. To further reveal the molecular characteristics of HPCs, we analyzed differentially expressed genes (DEGs) of 6 HPC clusters. We showed remarkably diverse transcriptional features within progenitor subtypes, characterized by the combinatorial or specific expression pattern of classic progenitor markers (VIM, NES, FABP7 and SLC1A3), proneural transcription factors (ASCL1, NHLH2 and DLX1) and new neural progenitors enriched candidates such as FAM107A, TTYH1 and HMGA2. The candidates were validated with immunostaining. In summary, our results demonstrated the molecular diversity of neural progenitor in mammalian hypothalamus.

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Deciphering the spatial-temporal molecular features of human developing hypothalamus at single-cell level

Project description:We revealed the molecular and cellular composition along spatial-temporal development of human hypothalamus by single-cell transcriptomic sequencing. The hypothalamus was manually micro-dissected from serial coronal 600-800μm thick slice using a vibratome. We excluded poor quality cells after the gene expression matrix was generated by Cell Ranger with Scanpy (V1.4.4) package. We identified 11 major transcriptomic types including neuroepithelium (NE), neural progenitors (NP), neurons, astrocytes, oligodendrocyte precursor cells (OPC), oligodendrocyte (OL), ependymocytes (Ependy), microglial cells, endothelial cells (Endoth), mural cells as well as vascular and leptomeningeal cells (VLMCs) that were characterzied with their respective classic markers. We uncovered molecular diversity of NP subtypes and constructed their developmental trajectory. We also identified various neuronal subpopulations mapped into distinct spatial location. Overall, our data provided cellular and molecular landscape of human hypothalamic development.

2021-12-07 | GSE169109 | GEO

Control of neurogenic competence in mammalian hypothalamic tanycytes [ATAC-seq]

Project description:Hypothalamic tanycytes, radial glial cells that share many features with neuronal progenitors, can generate small numbers of neurons in the postnatal hypothalamus, but the identity of these neurons and the molecular mechanisms that control tanycyte-derived neurogenesis are unknown. We report that tanycyte-specific disruption of the NFI family of transcription factors (Nfia/b/x) stimulates proliferation and tanycyte-derived neurogenesis. Single-cell RNA- and ATAC-Seq analysis reveals that NFI factors repress Shh and Wnt signaling in tanycytes, and small molecule inhibition of these pathways blocks proliferation and tanycyte-derived neurogenesis in Nfia/b/x-deficient mice. We show that Nfia/b/x-deficient tanycytes give rise to multiple mediobasal hypothalamic neuronal subtypes that can mature, integrate into hypothalamic circuitry, and selectively respond to changes in internal states. These findings identify molecular mechanisms controlling tanycyte-derived neurogenesis that can potentially be targeted to selectively remodel hypothalamic neural circuitry controlling homeostatic physiological processes.

2020-10-30 | GSE160375 | GEO

Control of neurogenic competence in mammalian hypothalamic tanycytes [RNA-seq]

2020-10-30 | GSE160377 | GEO

Transcriptional Profiling of rat hypothalamic response to TCDD

Project description:In many mammals, halogenated aromatic hydrocarbon (HAH) exposure causes wasting syndrome, defined as lethal weight loss as a result of severe and persistent hypophagia. The most potent HAH in causing wasting is 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD), which exerts its toxic effects through the aryl hydrocarbon receptor (AHR) – a transcription factor. Because TCDD toxicity is thought to predominantly arise from dysregulation of AHR-transcribed genes, we hypothesized that wasting syndrome is due to TCDD-induced dysregulation of genes involved in regulation of food-intake. We therefore focused on the hypothalamus, as it is the regulatory center of food-intake and energy balance in the central nervous system. We profiled mRNA abundance in hypothalamic tissue from two rat strains with widely differing sensitivities to wasting syndrome: TCDD-sensitive Long-Evans rats and TCDD-resistant Han/Wistar rats, 23 hours after exposure to TCDD (100 μg/kg) or corn oil vehicle. We found that TCDD exposure caused minimal transcriptional dysregulation effects in the hypothalamus, with only 6 genes changed in Long-Evans rats and 15 genes in Han/Wistar rats. Two of the most dysregulated genes were Cyp1a1 and Nqo1, which are induced by TCDD across a wide range of tissues and are considered sensitive markers of TCDD exposure. The minimal response of the hypothalamic transcriptome to a lethal dose of TCDD at an early time-point suggests that the hypothalamus is not the predominant site of initial events leading to hypophagia and associated wasting. TCDD may affect feeding behaviour via events upstream or downstream of the hypothalamus, and further work is required to evaluate this at the level of individual hypothalamic nuclei and subregions. Two strains, each with drug-treated vs vehicle-control

2014-12-23 | E-GEOD-61039 | biostudies-arrayexpress

Repeated hypoglycemia in diabetic mice induce hypothalamic mitochondrial and synaptic activity deregulations characteristic of neurodegenerative diseases

Project description:Repeated exposures to insulin-induced hypoglycemia in diabetic patients progressively impair the counter-regulatory response (CRR) that restores normoglycemia. This defect is characterized by reduced secretion of glucagon and other counter-regulatory hormones. Evidence indicates that glucose responsive neurons located in the hypothalamus, orchestrate the CRR. Here, we aimed at identifying the changes in hypothalamic gene and protein expression that underlie impaired CRR. High fat diet fed and low dose streptozocin-treated C57BL6N mice were exposed to one (acute hypoglycemia, AH) or multiple (recurrent hypoglycemia, RH) insulin-induced hypoglycemic episodes. Single nuclei RNA sequencing (snRNAseq) data were obtained from the hypothalamus and cortex of AH and RH mice. Proteomic data were also obtained from hypothalamic synaptosomal fractions. The present study shows that repeated moderate hypoglycemia in diabetic mice lead, in the hypothalamus, to multiple cellular physiology changes, affecting all cell types and their interactions, which show striking features of neurodegenerative diseases. It also shows that repeated hypoglycemic episodes affect very differently the hypothalamus and the cortex.

2023-11-13 | PXD040183 | Pride

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